MATERIAL AND METHODS: The systematic review was conducted in compliance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement guidelines. Relevant literature was searched from PubMed, Web of Science, Scopus and Ebscohost databases from inception until 31 August 2020. The risk of bias in each study was determined based on the Newcastle-Ottawa Scale tool. Results from random-effect meta-analyses were presented as summary estimates of odds ratios (ORs) for seropositivity and standardised mean difference (SMD) of autoantibody levels with 95% confidence intervals. Sensitivity tests and meta-regression were performed to assess the robustness of the results and potential cause of heterogeneity.
RESULTS: The electronic and manual searches gathered 932 articles. Following screening and full-text assessment, a total of 29 studies were included in the analysis. Twenty-eight published observational studies were included in the quantitative analysis in the form of random-effect meta-analysis which revealed that PD was associated with anti-citrullinated proteins autoantibodies (ACPAs) and Rheumatoid Factor (RF) seropositive RA patients (OR for ACPA seropositivity: 1.82; 95% CI: 1.13-2.93) (OR for RF seropositivity: 1.53; 95% CI: 1.05-2.24). Also, RA patients with PD had increased serum levels of ACPA and RF. However, high heterogeneity among studies' results, partially ascribed to the unstandardised case definition of PD and laboratory testing of autoantibodies. Apart from ACPA and RF in serum, studies which reported on other RA-related autoantibodies, as well as autoantibody levels in saliva and GCF were scarce.
CONCLUSION: RA patients with PD tend to have greater ACPA and RF levels in their serum when compared with the RA patients without PD supporting the plausible role of PD in the development of systemic autoimmunity in RA patients.
Patients and methods: This was a prospective study conducted in Hospital Pulau Pinang, Malaysia, between March 2015 and June 2015. Educational intervention was provided to 96 patients (11 males, 85 females; mean age 52.4±12.9 years; range, 20 to 83 years) who fulfilled the inclusion/exclusion criteria. Questionnaires to assess knowledge of CVD risk were given to patients to be answered before reading the informative leaflet, after one hour of intervention, and during their next follow-up three months from the intervention. Both the informative leaflet and questionnaires were prepared in English and then translated into Malay and Chinese languages to suit the need of local patients.
Results: Our results showed that RA patients had good knowledge at baseline regarding risk of smoking, hypertension, and hyperlipidemia on increasing CVD risk and that exercise would not damage their joints. However, they had low knowledge at baseline regarding the amount of exercise needed for lower CVD risks and risk of CVD with use of anti-inflammatory drugs in RA. Total knowledge score increased significantly from baseline immediately after educational intervention. However, total knowledge score decreased after three months compared to immediate post- intervention phase while it was still significantly higher compared to baseline. The improvement was most obvious for knowledge regarding anti- inflammatory drugs and CVD risk and knowledge regarding the number of flares and CVD risk. Our study did not find any significant association between demographic characteristics and traditional cardiovascular risk factors with knowledge of CVD risk.
Conclusion: Rheumatoid arthritis patients have low knowledge regarding their CVD risk related to their disease. The intervention of providing an informative leaflet effectively improved the knowledge of this group of patients on CVD risk particularly in the field related to RA-specific risk.
MATERIALS AND METHODS: Gingival tissue samples of healthy (n = 5), PD with RA (n = 5) and PD without RA (n = 5) were collected. Specimens were formalin fixed, paraffin embedded and sectioned at 4 μm. The tissue sections were analysed for the presence of citrullinated and carbamylated proteins by immunohistochemistry. Semi-quantitative analysis was performed to quantify and compare the protein abundance between groups.
RESULTS: The number of cells containing citrullinated and carbamylated proteins with higher intensity was markedly increased in gingival tissues from PD with or without RA in comparison with healthy controls.
CONCLUSION: Inflamed gingival tissue is a potential source of citrullinated and carbamylated proteins other than synovial tissues. The extent to which the local accumulation of these proteins contributes to the pathogenesis of RA needs further elucidation.
CLINICAL RELEVANCE: If PD is a potential source of post-translationally modified proteins, untreated PD should not be taken lightly in the context of RA. Hence, addressing gingival inflammation should be viewed as an important preventive measure in the general population not only for the progression of periodontal disease but also reducing the risk of developing extra-oral comorbidities.